Stents are generally placed within the lumen of a narrowed artery in cases when the outcome of angioplasty is uncertain, e.g. in the case of stenoses, recanalized occlusions or vessel dissection.
When a stent is unfolded, it applies a constant outward force on the vessel, maintaining the desired dimensions of the lumen and thus reducing the effects of stenosis.
However, recent studies on the subject prevealed that placement of a luminal endoprosthesis can cause injuries to the artery wall, which leads to what is called intimal hyperplasia.
The vascular wall is composed of three layers, namely the intima (innermost layer composed of a single layer of endothelial cells), the media (middle layer which is composed of smooth muscle cells, elastic sheets, elastic fibrils network and bundles of collagenous fibers) and the advantitia (the outer layer).
It is now well established that intimal hyperplasia is the main process that induces belated narrowing of the lumen, even one or two years after intervention. It is related to the loss of endothelium and to medial injuries, which lead to an accelerated luminal smooth muscles proliferation migrating from the media or the intima and later to atherosclerosis degeneration.
Presently, studies to reduce what is called intimal hyperplasia (small muscle tissue proliferation which leads to restenosis) are aimed at anti-proliferation or anti-mitotic drugs that are fixed on the stent surface via a polymer matrix.
These methods suffer from several difficulties:                the non uniformity of polymer surface and consequently the lack of consistency of the local drug delivery.        the lack of consistency of the kinetic degradation of the polymer matrix.        the stability of the polymer fixation on the surface of the stent.        the determination of the right value of the drug dose to be affixed on the matrix.        
The drugs used are similar to those which are used as anti-cancer drugs, e.g. Taxol and Rapamycin. The use of high amounts of these molecules could be very harmful for the patient.
The restenosis of the stent induced by intimal hyperplasia poses a major problem for stent efficiency, mainly for arteries such as femorals, internal carotids or coronaries.
For the femoral artery, for example, many clinical trials show that stents give poor results due to the restenosis which is a consequence of intimal hyperplasia; 50 to 60% failure.
A new approach showed that the restenosis was bound to unexpected mechanical problems.
Femoral Artery:
A low shear stress along the cell wall is considered as an important factor of atherosclerotic plaque formation. It has been correlated with intimal thickening and has been shown to alter endothelial cells structure and function.
The disturbed flow increases cell turnover particularly in the areas of low blood velocity, which could explain the loss of contact inhibition of cell growth.
Internal Carotid:
The human carotid bifurcation is another example where flow model studies have demonstrated that the intimal plaques form in the low shear stress region of the carotid sinus opposite the flow and not in the high shear stress region along the inner wall of the carotid artery.
Coronary Artery
Similarly, the low shear stress is now shown to be a main cause of plaques formation at the branch points just distal to the bifurcation of the left main coronary artery into LAD and circumflex. This region exhibits a low blood flow velocity and a low shear stress, in other words the coronary artery tree demonstrates also a relationship between the shear stress and plaque formation.
The coronary arteries are subject to two systolic phases and one diastolic flow episode during each cardiac cycle, thus potentially placing them at a higher risk rank than systemic arteries to atherosclerosis. Shear stress oscillation is directly influenced by heart rate. At higher rate, coronary arteries are exposed to more acute oscillatory than at low shear stress episodes, which accelerate the formation of atherosclerosis plaques. For example, an increase in the mean heart rate from 70 to 80 beats/min would result in an increase of over 5 million heart beats per year. The duration of the systolic phase is generally constant for varying heart rates, whereas the duration of diastolic phase shortens with increasing heart rates.
It is important to mention that the effect of heart rate on atherosclerosis is associated with carotid artery atherosclerosis.
Many stents are well known and are described in the prior art.
In WO 01/01887, it is disclosed a composite stent which comprises an inner PTFE tubular structure and an outer PTFE tubular structure assembled about the inner structure and between these two structures is interposed a distensible stent. Thus, this layered structure improves both axial and radial compliance of the stent.
The invention described in WO 02/47579 concerns a prosthesis for blood vessels whose frame comprises a plurality of interconnected layers which are formed of two interwoven frame wires. This configuration allows increasing both the stability and the strength of the stent.
However there is no document in the prior art which discloses the feature of the present invention to favour blood flow.